首页|铜代谢紊乱介导非酒精性脂肪性肝病合并肌少症的研究进展

铜代谢紊乱介导非酒精性脂肪性肝病合并肌少症的研究进展

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非酒精性脂肪性肝病(non-alcoholic fatty liver disease)与肌少症(sarcopenia)是与年龄有关的常见慢性病共病,二者存在众多共同的病理生理因素,其潜在相关机制尚未完全阐明.近年来铜死亡作为一种新型细胞死亡方式被发现,铜稳态(copper homeostasis)在多种慢性疾病中的潜在功能角色成为当前的研究热点.肝脏内铜元素的缺失与早期非酒精性脂肪性肝病的发生密切相关,而骨骼肌内铜过载可能通过多种信号途径促进肌少症的发生,以铜蓝蛋白为代表的血清铜形成的细胞外铜过载在此过程中扮演着潜在性的功能角色.本篇综述从铜代谢角度出发阐述了铜稳态失衡与早期非酒精性脂肪性肝病合并肌少症发病的可能机制,以期为临床早期改善甚至逆转这两种代谢性疾病提供分子靶点和理论基础.
Research Progress on Copper Metabolism Disorders-Mediated Non-Alcoholic Fatty Liver Disease Combined with Sarcopenia
Non-alcoholic fatty liver disease(NAFLD)and sarcopenia are common age-related chronic comorbidities that share many common pathophysiological factors.However,their un-derlying mechanisms have not been fully elucidated.In recent years,cuproptosis has been discov-ered as a new cell death mode,and the potential functional role of copper homeostasis in a variety of chronic diseases has become a research focus.Loss of copper in the liver is closely related to the occurrence of early NAFLD,and copper overload in skeletal muscles may promote the occur-rence of sarcopenia through various signaling pathways.As indicated by ceruloplasmin levels in serum,extracellular copper overload may play a potential functional role in this process.This re-view discusses the possible mechanism of copper homeostasis imbalance and the onset of early NAFLD combined with sarcopenia from the perspective of copper metabolism,in order to provide molecular targets and theoretical basis for early clinical improvement or even reversal of these two metabolic diseases.

non-alcoholic fatty liver diseasesarcopeniacoppercopper homeostasiscupropto-siscopper metabolismceruloplasminoxidative stress

李畅、杨威、邓云锋、陈宁、范晶晶

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武汉体育学院运动医学院,武汉 430079

长沙卫生职业学院公共教学部,长沙 410100

武汉体育学院运动训练监控湖北省重点实验室,武汉 430079

非酒精性脂肪性肝病 肌少症 铜稳态 铜死亡 铜代谢 铜蓝蛋白 氧化应激

国家自然科学基金国家自然科学基金湖北省自然科学基金武汉体育学院中青年科研团队项目湖北省教育厅科研项目中青年人才项目

32071176817013912023AFB70021KT08Q20224104

2024

生理科学进展
中国生理学会,北京大学

生理科学进展

CSTPCD北大核心
影响因子:0.635
ISSN:0559-7765
年,卷(期):2024.55(2)
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